Homeostasis

• External environment changes effect the internal environment.
• Keeping your internal environment constant is vital to stop cells from malfunctioning/being damaged, and homestasis does just this.
• Especially important to maintain temperature (too high & enzymes can become denatured, too low & the enzyme activity is reduced-optimum 37'C) and pH (too high/low then enzymes are denatured- optimum is pH7)
• Glucose concentration is also an important factor to maintain. Too high- water potential reduced so H2O molecules diffuse by osmosis out of cells into blood (cells shrivel up & die) Too low- cells stop working as there's not enough glucose to provide energy.

Negative feedback:

• Receptors detect when a level is too high/low, info is sent via nervous/hormonal system to the effectors, which counteract the change.
• This is negative feedback, which brings all the levels back to normal.
• Multiple feedback systems mean a faster return to normal, as it actively increases/decreases a level e.g. in a car, take foot off accelerator slows you down, but using the brake aswell would slow you down a lot faster.

Positive Feedback:

• Amplifies any change to levels.
• Positive feedback makes the levels which have changed fluctuate further away from the norm.
• Useful to quickly activate something e.g. blood clot
• Not involved in homeostasis as it doesn't keep environment constant.

Hypothermia:

• Low body temperature (below 35'C)
• Result of heat being lost from the body faster than it's being produced.
• Brain stops working properly, shivering stops making body even colder.
• Positive feedback makes body temperature drop even further (going away from the norm temperature) unless help is found.

Ectotherms (e.g. reptiles/fish):

• Can't control temperature internally, change behaviour instead-go in sun etc
• Internal temperature depends on their external surroundings.
• More active at higher temperatures & less active at low temperatures.
• Variable metabolic rate, don't generate a lot of heat themselves.

Endotherms (e.g. mammals/birds):

• Control body temperature internally & by behaviour (by finding shade etc).
• Internal temperature less affected by external temperature (up to a point).
• Can be active at any external temperature (up to a point).
• high metabolic rate & generate a lot of heat from metabolic reactions.

Heat Loss:

• Sweating- secreted from sweat glands, then evaporates, cooling skin.
• Hairs lie flat- erector pili muscles relax, less air is trapped- more heat lost.
• Vasodilation- arterioles near surface dilate and more blood flows through capillaries, so more heat is lost by radiation.

Heat Production:

• Shivering- muscles contract in spasms, more heat is produced (increased rate of respiration).
• Hormones- adreneline released- increases metabolic rate- more heat.

Heat Conservation:

• Less sweat- reduced amount of heat loss.
• Hairs stand up-erector pili muscles contract, hairs trap air& insulate body.
• Vasoconstriction- arterioles constrict, less blood flows, reduces heat loss.

• Part of the brain (the hypothalmus) maintains a constant body temperature.
• Gets info about both internal & external temperature from thermoreceptors.
• Internal temperature info is from thermoreceptors in hypothalmus which detect blood temperature.
• External temperature info is from thermoreceptors in skin which detect skin temperature.
• Thermoreceptors send impulses along sensory neurones to hypothalmus, which sends impulses along motor neurones to effectors (muscles/glands).
• All unconcious- via the autonomic nervous system.
• Effectors use methods shown on the previous card ("mammalian methods...") to return temperature to normal (i.e. 37'C).

• Cells in pancreas monitor blood glucose concentration (BGC)
• BGC rises after eating carbohydrates (get energy from these) and falls after exercise (more glucose is used in respiration to produce energy).
• Controlled by the hormones insulin & glucagon (negative feedback)
• Beta cells secrete insulin & alpha cells secrete glucagon.

Insulin Lowers BGC when it's too high...

• Binds to receptors in liver & muscle cells and increases the permeability to glucose, so cells take up more glucose.
• Also activates enzymes which convert glucose into glycogen (glycogenesis).
• Increases rate of respiration of glucose, esp. in muscle cells.

Glucagon raises BGC when it's too low...

• Binds to specific receptors in liver cells, activates enzymes which convert glycogen into glucose (glycogenolysis) and also converts amino acids into glucose (gluconeogenesis)
• Glucagon decreases rate of respiration of glucose in cells.

Adrenaline:

• Hormone which is secreted from adrenal glands (above your kidneys) when there's a low blood glucose concentration (BCG)
• Binds to receptors in liver cell membranes
• Activates glycogenolysis (glycogen --> glucose)
• Inhibits glycogenesis (glucose --> glycogen)
• Inhibits insulin secretion & activates glucagon secretion.
• Body is ready for action as it has more glucose available for muscles to use in respiration.

Can also activate glycogenolysis inside a cell...

• Adrenaline& glucagon bind to receptors- activate adenylate cyclase enzyme.
• Enzyme converts ATP into a chemical messenger ("second messenger").
• Second messenger called cyclic AMP (cAMP).
• cAMP activates chain of reactions: glycogen --> glucose (glycogenolysis)

Diabetes is when blood glucose concentration can't be controlled properly...

Type 1:

• Beta cells (in islets of langerhans) don't produce any insulin
• After eating, BGC levels rise&stay high-hyperglycaemia- can end in death.
• Kidneys can't reabsorb extra glucose, so some of it is excreted in urine.
• Injections help treat this, but too many and hypoglycaemia can occur (dramatic drop in BGC levels). Eating regularly & less sugar also helps.

Type 2:

• Usually aquired later in life- linked to obesity.
• Beta cells don't produce enough insulin/ body cells dont respond properly to insulin (e.g. their insulin receptors on membranes don't work.)
• Results in cells not taking up enough glucose, so BGC levels are high.
• Treated by losing weight and controlling amount of sugars eaten.

• Follicle develops in the ovary.
• Ovulation- egg is released.
• Uterus lining thickens so fertilised egg can implant.
• Corpus luteum (corp lut.) develops from follicle remains.
• No fertilisation- lining breaks down & leaves body (menstruation).

Hormones:

• Follicle-stimulating hormone (FSH)- stimulates follicle to develop.
• Luteinising hormone (LH)- stimulates ovulation & development of corp lut.
• Oestrogen (O)- stimulates thickening of uterus
• Progesterone (P)- maintains thick uterus lining
• FSH & LH secreted by anterior pituitary gland. O & P secreted by ovaries.

• High FHS- follicle develops- releases O. FSH stimulates ovaries to release O
• O conc. rises- stimulates lining to thicken. Inhibits FSH being released.
• O conc. peaks- stimulates pituitary gland to release LH and FSH.
• Surge of LH- stimulates ovulation. Corp lut. develops & releases P.
• P conc. rises- inhibits FSH & LH release. Lining maintained. No fertilisation- corp lut. breaks down & stops releasing P.
• P conc. falls- FSH & LH conc. increase (no longer inhibited by P). Lining isn't maintained, so it breaks down & leaves body (menstruation).

Negative Feedback:

• FSH stimulates release of O. O inhibits release of FSH.- no more follicles!
• LH stimulates corp. lut to develop producing P, P inhibits release of LH- no more follicles develop & lining broken down if no fertilisation occurs.

Positive feedback:

• O stimulates release of LH, which stimulates release of more O etc etc.